FatherOf2 wrote:We re-started Piracetam last Sunday, after 5 months of trying different treatments. Again, we are seeing a remarkable improvement: much more eye contact, much more attention (as if my son woke up), much more verbal and more spontaneous speech, using longer sentences, which are also appropriate. But, visual and verbal stimming, hyperactivity, reacting to his name and following multi-step directions are and have been our biggest issues. Even GABA and magnesium don't help. I feel that chelation might be the missing piece in our puzzle. But, before I do that, I need to make sure we have no yeast left.

Some time ago, CaringDad71 posted here Dr. Yasko's message indicating that Piracetam, due to its stimulation of NMDA receptors, "may create additional excitotoxin damage" (http://www.autismweb.com/forum/viewtopic.php?f=4&t=23185). But, the prevalant opinion is that Piracetam is a neuroprotector, in fact, a very strong one.

1.--Mitochondrial dysfunction including decrease of mitochondrial membrane potential and reduced ATP production represents a common final pathway of many conditions associated with oxidative stress, for example, hypoxia, hypoglycemia, and aging. 2.--Since the cognition-improving effects of the standard nootropic piracetam are usually more pronounced under such pathological conditions and young healthy animals usually benefit little by piracetam, the effect of piracetam on mitochondrial dysfunction following oxidative stress was investigated using PC12 cells and dissociated brain cells of animals treated with piracetam. 3.--Piracetam treatment at concentrations between 100 and 1000 microM improved mitochondrial membrane potential and ATP production of PC12 cells following oxidative stress induced by sodium nitroprusside (SNP) and serum deprivation. Under conditions of mild serum deprivation, piracetam (500 microM) induced a nearly complete recovery of mitochondrial membrane potential and ATP levels. Piracetam also reduced caspase 9 activity after SNP treatment. 4.--Piracetam treatment (100-500 mg kg(-1) daily) of mice was also associated with improved mitochondrial function in dissociated brain cells. Significant improvement was mainly seen in aged animals and only less in young animals. Moreover, the same treatment reduced antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase, and glutathione reductase) in aged mouse brain only, which are elevated as an adaptive response to the increased oxidative stress with aging. 5.--In conclusion, therapeutically relevant in vitro and in vivo concentrations of piracetam are able to improve mitochondrial dysfunction associated with oxidative stress and/or aging. Mitochondrial stabilization and protection might be an important mechanism to explain many of piracetam's beneficial effects in elderly patients.

Piracetam is a prototype of nootropic drugs used to improve cognitive impairment. However, recent studies suggest that piracetam can have analgesic and anti-inflammatory effects. Inflammatory pain is the result of a process that depends on neutrophil migration, cytokines and prostanoids release and oxidative stress. We analyze whether piracetam has anti-nociceptive effects and its mechanisms. Per oral pretreatment with piracetam reduced in a dose-dependent manner the overt pain-like behavior induced by acetic acid, phenyl-p-benzoquinone, formalin and complete Freund's adjuvant. Piracetam also diminished carrageenin-induced mechanical and thermal hyperalgesia, myeloperoxidase activity, and TNF-α-induced mechanical hyperalgesia. Piracetam presented analgesic effects as post-treatment and local paw treatment. The analgesic mechanisms of piracetam were related to inhibition of carrageenin- and TNF-α-induced production of IL-1β as well as prevention of carrageenin-induced decrease of reduced glutathione, ferric reducing ability and free radical scavenging ability in the paw. These results demonstrate that piracetam presents analgesic activity upon a variety of inflammatory stimuli by a mechanism dependent on inhibition of cytokine production and oxidative stress. Considering its safety and clinical use for cognitive function, it is possible that piracetam represents a novel perspective of analgesic.

From the abstract above, "The analgesic mechanisms of piracetam were related to inhibition of carrageenin- and TNF-α-induced production..." Interestingly, the alpha7 nicotine acetylcholine receptors, which are mutated in my son, are supposed to inhibit TNF production. This perhaps explains why my son reacts so positively to Piracetam - it compensates for the lack of these receptors.

We studied the role of oxidative stress and the effect of vinpocetine (1.5, 3 or 6 mg/kg) and piracetam (150 or 300 mg/kg) in acute demyelination of the rat brain following intracerebral injection of ethidium bromide (10 �l of 0.1%). Results: ethidium bromide caused (1) increased malondialdehyde (MDA) in cortex, hippocampus and striatum; (2) decreased total antioxidant capacity (TAC) in cortex, hippocampus and striatum; (3) decreased reduced glutathione (GSH) in cortex and hippocampus (4); increased serum nitric oxide and (5) increased striatal (but not cortical or hippocampal) acetylcholinesterase (AChE) activity. MDA decreased in striatum and cortex by the lower doses of vinpocetine or piracetam but increased in cortex and hippocampus and in cortex, hypothalamus and striatum by the higher dose of vinpocetine or piracetam, respectively along with decreased TAC. GSH increased by the higher dose of piracetam and by vinpocetine which also decreased serum nitric oxide. Vinpocetine and piracetam displayed variable effects on regional AChE activity.

The present study investigates the potential of Piracetam and Vinpocetine (nootropic drugs, known to possess neuroprotective properties) in preventing hypoxia-reoxygenation induced oxidative stress in primary hippocampal cell culture. The hippocampal culture was exposed to hypoxia (95% N(2), 5% CO(2)) for 3h and followed by 1h of reoxygenation (21% O(2) and 5% CO(2)) at 37 °C. The primary hippocampal cultures were supplemented with the optimum dose of Piracetam and Vinpocetine, independently, and the cultures were divided into six groups, viz. Control/Normoxia, Hypoxia, Hypoxia+Piracetam, Hypoxia+Vinpocetine, Normoxia + Piracetam and Normoxia+Vinpocetine. The cell-viability assays and biochemical oxidative stress parameters were evaluated for each of the six groups. Administration of 1mM Piracetam or 500 nM Vinpocetine significantly prevents the culture from hypoxia-reoxygenation injury when determined by Neutral Red assay, LDH release and Acetylcholine esterase activity. Results showed that Piracetam and Vinpocetine supplementation significantly prevented the fall of mitochondrial membrane potential, rise in ROS generation and reduction in antioxidant levels associated with the hypoxia-reoxygenation injury. In conclusion, the present study establishes that both Piracetam and Vinpocetine give neuroprotection against hypoxia-reoxygenation injury in primary hippocampal cell culture.

We just started using a little noopept which is sorta in the racetam family and I think we are seeing a little bit of an improvement. I definitely want to try piracetam myself and also there is a fat-soluble analog of piracetam that I want to try too.

No scientific evidence that autism has a toxic or allergic basis. - Mr. Barrett

This combination is probably the most popular stack used by nootropic buffs. Piracetam, what is also known as Nootropyl or Lucetam, works by improving the functioning of (ACh) transmitters and receptors. Though primarily prescribed by doctors for people suffering from Alzheimer's, depression, and even schizophrenia, it is used off-label by healthy adults as a way to boost acetylcholine function — what is an important neurotransmitter. But in order to experience its benefits, including increased mental clarity, spatial memory, and an overall boost in brain functioning, choline needs to be ingested along with it. Choline, as a water-soluble essential nutrient, works with the Piracetam and is often used to prevent headaches that is sometimes associated with its use (see, this is why we told you to see a doctor before trying any of this stuff). An effective dose would be 300 mg of Piracetam plus 300 mg of Choline three times per day (about every four hours or so). Those willing to step it up a bit can also try the Focus XT + Piracetam stack. And interestingly, Piracetam is a popular supplement in the subculture of lucid dreaming.

Yasko's against it? Fantastic -- I just received my shipment of Piracetam. I've pretty much stopped all supplements for now because of liver function issues and issues with low free iron and high ferritin (very, very long story that I'm still trying to get to the bottom of), so if I do any supps right now, it has to be one that I REALLY want to do. And if Yasko's against this one -- this is one I'm definitely gonna try.

We had tried vinpocetine before and we saw definite gains in speech from it, but we ran out of something -- and I think that something was choline. Another amazing mom just told me about using CDP choline with vinpocetine or piracetam. I had a bottle of citocoline in my cupboard that I'd been meaning to try but I just never really knew what to do with it. I just started it and it does really amazing things for speech. I mean...Fan. Freaking. Tastic. Maia told me, "I wanted to talk to 'ebeyone' today." It seemed to increase the desire to want to speak to others. I haven't introduced the piracetam yet.

However, I will note that past a certain dosage, we saw some deteriorating emotional regulation -- but when I looked up the citicoline pathway, it does require a lot of magnesium. I might not do the high dose magnesium right now because of the liver issues, but, yeah, citicoline needs magnesium or you might see some emotional regulation issues creeping in -- but when I upped the magnesium, the citicoline does do some really awesome things for speech.

Yasko's not against piracetam. She says on her forum that some people do well with it, but that she prefers ampamet and to make sure glutamate/Gaba are in balance. Using either drug if glutamate is too high can produce more stims.

alberta wrote:Yasko's against it? Fantastic -- I just received my shipment of Piracetam. I've pretty much stopped all supplements for now because of liver function issues and issues with low free iron and high ferritin (very, very long story that I'm still trying to get to the bottom of), so if I do any supps right now, it has to be one that I REALLY want to do. And if Yasko's against this one -- this is one I'm definitely gonna try.

We had tried vinpocetine before and we saw definite gains in speech from it, but we ran out of something -- and I think that something was choline. Another amazing mom just told me about using CDP choline with vinpocetine or piracetam. I had a bottle of citocoline in my cupboard that I'd been meaning to try but I just never really knew what to do with it. I just started it and it does really amazing things for speech. I mean...Fan. Freaking. Tastic. Maia told me, "I wanted to talk to 'ebeyone' today." It seemed to increase the desire to want to speak to others. I haven't introduced the piracetam yet.

However, I will note that past a certain dosage, we saw some deteriorating emotional regulation -- but when I looked up the citicoline pathway, it does require a lot of magnesium. I might not do the high dose magnesium right now because of the liver issues, but, yeah, citicoline needs magnesium or you might see some emotional regulation issues creeping in -- but when I upped the magnesium, the citicoline does do some really awesome things for speech.

I don't think Yasko is against piracetam. She just assumed that it is a stimulator of NMDA receptors and, thus, by definition, is an excitotoxin. I don't think scientists know exactly how piracetam works, and they cautiously use the words "modulate" or "regulate" rather than "stimulate". If piracetam killed neurons by overstimulating them, it wouldn't have such safety profile even in huge doses and it wouldn't have been used to treat cognitive impairments in older adults. You will find that some doctors warn against choline too, saying that too much choline leads to overstimulated neurons. Piracetam indeed depletes acetylcholine in the brain and needs supplementation of choline (CDP choline, phosphatidylcholine, or alpha GPC, which I've read has superior bioavalaibility).

Last edited by FatherOf2 on Sat May 11, 2013 12:10 am, edited 1 time in total.

In vitro preincubation of brain membranes of aged mice with piracetam (0.1-1.0 mmol/L) enhanced membrane fluidity, as indicated by decreased anisotropy of the membrane-bound fluorescence probe 1,6-diphenyl-1,3,5-hexatriene (DPH). Piracetam had similar in vitro effects on brain membranes of aged rats and humans, but it did not alter brain membrane fluidity in young mice. Chronic treatment of young and aged rats with piracetam (300 mg/kg once daily) significantly increased membrane fluidity in some brain regions of the aged animals, but had no measurable effect on membrane fluidity in the young rats. The same treatment significantly improved active avoidance learning in the aged rats only. It is suggested that some of the pharmacological properties of piracetam can be explained by its effects on membrane fluidity.

Extensive research of the recent years has demonstrated that piracetam is effective in the treatment of cognitive decline in aging and dementia. It is usually much more active in situations of impaired brain function. Accordingly, its mechanism of action has been associated with neurochemical deficits of the aged brain relevant to cognitive dysfunctions. Since many of these neurochemical deficits depend on changes of membrane properties, including fluidity, it is of special importance that piracetam not only modifies membrane properties by interacting with the polar head moieties of the phospholipid bilayer, but also that this effect is more pronounced in membranes of aged as opposed to young animal and human brains, and that this mechanism also has specific relevance for brain membranes of Alzheimer's disease patients. Altering membrane properties might also be involved in vascular effects of piracetam such as improved erythrocyte deformability and normalization of hyperactive platelet aggregation. This novel mechanism of piracetam thus combines a rather non-specific physico-chemical mode of action with the pharmacological and clinical experience with this unique drug - effects are always much more pronounced when function is impaired.

Subchronic treatment of aged mice with piracetam (500 mg/kg p.o. for 14 days) elevates N-methyl-D-aspartate (NMDA) receptor density by about 20% and normalizes the enhanced affinity of L-glutamate for the NMDA receptor. Since deficits at the level of the NMDA receptor might be one of the mechanisms underlying age-associated cognitive impairment, the effects reported for piracetam may be relevant for the cognition-enhancing properties of this drug

So, pirecetam only affects neurons if their function is impaired, and it does so by helping them to regain that function (increases fluidity of their membrane if it is too low). Healthy subjects don't respond to piracetam. You would expect healthy people to respond to piracetam if it was simply a stimulator of NMDA receptors. So, the fact that my son positively reacts to piracetam means that something is wrong with his NMDA receptors (they control memory, which is significantly impaired in my son). I, as a healthy adult, have absolutely no response to piracetam (tried it many times in different doses). Nevertheless, I would advise to proceed cautiously, by starting at 50mg/kg dose, which is what my son has been taking and it already helps at that small dose.

Last edited by FatherOf2 on Sat May 11, 2013 12:11 am, edited 1 time in total.

According to the mentioned studies, Piracetam increases membrane fluidity. From wikipedia: "membrane fluidity refers to the viscosity of the lipid bilayer of a cell membrane. The membrane phospholipids incorporate fatty acids of varying length and saturation. Shorter-chain fatty acids, and ones with greater unsaturation (read Omega 3 EFAs), are less stiff, less viscous and have lower melting points." From a different source: "Omega-3 EFAs are distributed heavily throughout cell membranes in the body and help make the membranes more fluid... Fluidity of cell membranes is essential for cell regeneration, detoxification, and optimal receptor function. Membrane fluidity is especially important for efficiency of brain performance." From another source: "The more polyunsaturated lipids contained within the membrane, the greater its fluidity, and the greater its ability to dynamically change its organisation to suit its environment and optimise cellular function." More about membrabe fluidity and EFAs is here: http://www.kidshealth-central.com/omega-3-the-fats-that-have-everybody-smiling.html.

Fantastic info, FatherOf2! I'm really excited about starting piracetam now. That is exactly what I want -- membrane fluidity. I've come across piracetam a few times for acetylcholine production, which we could use. But I am trying to increase cell membrane fluidity too -- for a lot of reasons that I won't get into because it's just too long of a story to get into...but I think this is exactly what I'm looking for.

So, pirecetam only affects neurons if their function is impaired, and it does so by helping them to regain that function (increases fluidity of their membrane if it is too low). Healthy subjects don't respond to piracetam. You would expect healthy people to respond to piracetam if it was simply a stimulator of NMDA receptors. So, the fact that my son positively reacts to piracetam means that something is wrong with his NMDA receptors (they control memory, which is significantly impaired in my son). I, as a healthy adult, have absolutely no response to piracetam (tried it many times in different doses).

Really interesting information. My son used this when he was probably 4 or 5 years old. We saw a boost initially. I ran out and didn't order it again for quite a while because I was trying so many other things. When I introduced it many years later, no response- good or bad. With what you wrote, this makes sense.

Yesterday was a great day. We stopped LDN for just a day, upped his Piracetam to 1.2g (still below the minimum dose of 100mg/kg), rubbed Lee Silsby B-complex/B6/B12 creams, gave him fish oil and 200mg of magnesium as we usually do. We went to the zoo and observed a much less anxious, more confident behavior. He walked like a regular boy (much less on toes as he usually does). For the first time, he curiously looked at the scenery below when riding a cable car (before, he would just sit still and stare in space being uninterested). He didn't have melt downs as he usually did, no stopping and dropping to the ground and screaming when you try to pick him up. Still ways to go (stimming and hyperactivity being major issues), but so far I am impressed. My wife even wanted to give Piracetam to his NT twin brother. I said "no". We also had a first session of iLS on Friday. We think that part of the improved behavior (especially more confident walking, going up/down stairs) is due to it. By the way, some people use Piracetam to reduce social anxiety.

FatherOf2 wrote:Yesterday was a great day. We stopped LDN for just a day, upped his Piracetam to 1.2g (still below the minimum dose of 100mg/kg), rubbed Lee Silsby B-complex/B6/B12 creams, gave him fish oil and 200mg of magnesium as we usually do. We went to the zoo and observed a much less anxious, more confident behavior. He walked like a regular boy (much less on toes as he usually does). For the first time, he curiously looked at the scenery below when riding a cable car (before, he would just sit still and stare in space being uninterested). He didn't have melt downs as he usually did, no stopping and dropping to the ground and screaming when you try to pick him up. Still ways to go (stimming and hyperactivity being major issues), but so far I am impressed. My wife even wanted to give Piracetam to his NT twin brother. I said "no". We also had a first session of iLS on Friday. We think that part of the improved behavior (especially more confident walking, going up/down stairs) is due to it. By the way, some people use Piracetam to reduce social anxiety.

Yes. There's also a forum about Social Anxiety, where Piracetam is the main subject.

luis wrote:Fatherof2: Do you give the 1.2 g in divided doses, or all together ?

Divided. Half in the morning, half at noon. Today was ok day, not as good as yesterday (may be LDN had a bad effect). It is always like that with my son: one day is awesome, making me feel that from now on every day will be at least as good as that day or better, but the next day is down and I feel depressed. I need a lot of patience.I am considering adding TD NAC to my protocol to boost glutathione and reduce glutamate. Hopefully that would reduce stimming and help to detox.

luis wrote:Fatherof2: Do you give the 1.2 g in divided doses, or all together ?

Divided. Half in the morning, half at noon. Today was ok day, not as good as yesterday (may be LDN had a bad effect). It is always like that with my son: one day is awesome, making me feel that from now on every day will be at least as good as that day or better, but the next day is down and I feel depressed. I need a lot of patience.I am considering adding TD NAC to my protocol to boost glutathione and reduce glutamate. Hopefully that would reduce stimming and help to detox.

It should help. Magnesium is key to control glutamate.I wish you the best. Keep working !

DS has been on a product called Get Smart for about a week now. So far, the jury's still out on this one. We are seeing some great things (improved eye contact, speech attempts, improved cognitive ability, more awareness) but we are also seeing some negatives (aggression, easily frustrated, waking up throughout the night). I am not sure if the negative is due to a yeast flare-up, or from the Get Smart.

Pyritinol has been used in Europe since 1961 for various cognitive conditions such as dementia, head injury, stroke aftermath, coma, and cerebral circulatory disorders.Pyritinol has shown to help Attention Deficit Disorder (ADD) and is used by people of all ages to improve memory, concentration, and to enhance information processing.

Picamilon is a Russian nootropic that enhances cerebral circulation. Picamilon is used in Russia to treat anxiety, depression, headaches, glaucoma, and eye disorders.

Aniracetam and Oxiracetam are nootropics that improve communication between the two brain hemispheres.

Idebenone increases Nerve Growth Factor (NGF) in the brain. Idebenone has been used to treat Alzheimer's disease and to lessen brain damage from strokes. Idebenone protects the brain from excitotoxins like MSG and aspartame.

Vinpocetine is a periwinkle plant extract that: 1. dilates the arteries of the brain 2. improves Tinnitus (ringing in the ears) and Vertigo (dizziness). 3. can prevent stroke and reduce damage in following stroke.

Huperzine A (Huperzia serrata) is an ingredient found in Chinese Moss that enhances mental functioning by prolonging the life of the brain neurotransmitter acetylcholine. It works by inhibiting acetylcholinesterase, the enzyme that breaks down acetylcholine. This is the same mechanism of action by which the prescription drug Aricept works. Aniracetam 800mg

mamato3 wrote:DS has been on a product called Get Smart for about a week now. So far, the jury's still out on this one. We are seeing some great things (improved eye contact, speech attempts, improved cognitive ability, more awareness) but we are also seeing some negatives (aggression, easily frustrated, waking up throughout the night). I am not sure if the negative is due to a yeast flare-up, or from the Get Smart.This is what is in the product: http://smart-nutrition.net/Get-Smart.htm

It is probably the result of higher self-awareness. But the disturbed sleep is not good. The stuff in this formula seems very potent. I would be concerned to give so many "smart" ingeredients at the same time. Also, check their address: 1765 Garnet #66, San Diego, CA 92109 on Google maps. I see a small apartment building in a poor neighborhood (can judge by the bars on windows) with a front sign LiveScan. Obviously, this is a one-man operation from his apartment. I would call and ask a question where do they make their stuff. If this is where they make it, I would be concerned.